Effect Of Lidocaine Infusion Research Articles

Effects of Lidocaine Infusion on Quality of Recovery and Agitation after Functional Endoscopic Sinus Surgery: Randomized Controlled Study

Background: After functional endoscopic nasal surgery, emergence agitation is not uncommon. The aim of this trial was to investigate the effect of perioperative lidocaine infusion on postoperative early recovery quality and incidence of emergence agitation in patient undergoing functional endoscopic sinus surgery. Study Design: Prospective, randomized, double-blinded, placebo-controlled trial. Methods: 100 patients of ASA I and II, aged 18 - 50 years, of both sexes scheduled for FEES, were assigned into two groups. In Group L; patients received an intravenous bolus infusion of 1.5 mg/kg lidocaine just before induction of anesthesia followed by a continuous infusion of 2 mg/kg/h during the operation and until the end of the surgery. In Group C; patients received normal saline infusion with the same volume as group L according to the same protocol. The primary endpoints were incidence of emergence agitation and postoperative recovery quality (QoR-40) score on first postoperative day (POD1). Results: Incidence of emergence agitation was significantly lower in group L (P 0.05) compared with group C. Global QoR-40 scores on POD1 were significantly lower in both groups compared with preoperative assessment, it was significantly higher in group L on POD1 (P 0.05) than in group C. Among the five dimensions of QoR-40, the scores for physical comfort and pain were superior in group L compared to group C (P 0.05) at POD1. Conclusion: Systemic lidocaine infusion can improve QoR-40 scores and decrease incidence of emergence agitation in patients scheduled for FEES, also it reduces the duration of stay in PACU after surgery.

Systemic Effects of Lidocaine Infusion for TAP Block Catheter

Systemic Effects of Lidocaine Infusion for TAP Block Catheter

The Effect of Lidocaine Infusion on theAcute Pain after the Surgery of Tibia Fracture under General Anesthesia

The Effect of Lidocaine Infusion on theAcute Pain after the Surgery of Tibia Fracture under General Anesthesia

Effects of Lidocaine Infusion during Experimental Endotoxemia in Horses

The clinical efficacy of IV infusion of lidocaine for treatment of equine endotoxemia has not been studied. Lidocaine infusion after exposure to lipopolysaccharide (LPS) will inhibit the inflammatory response and have inhibitory effects on the hemodynamic and cytokine responses to endotoxemia. Twelve horses. Two equal groups (n=6): saline (GI) and lidocaine (GII). In all animals, endotoxin (500 ng/kg body weight [BW]) was injected intraperitoneally over 5 minutes. Twenty minutes later, animals received a bolus of GI or GII (1.3 mg/kg BW) over 5 minutes, followed by a 6-hour continuous rate infusion of GI or GII (0.05 mg/kg BW/min). Treatment efficacy was judged from change in arterial blood pressure, peripheral blood and peritoneal fluid (PF) variables (total and differential cell counts, enzyme activities, and cytokine concentrations), and clinical scores (CS) for behavioral evidence of abdominal pain or discomfort during the study. Compared with the control group, horses treated with lidocaine had significantly lower CS and serum and PF tumor necrosis factor-alpha (TNF-alpha) activity. At several time points in both groups, total and differential cell counts, glucose, total protein and fibrinogen concentrations, and alkaline phosphatase, creatine kinase, and TNF-alpha activities were significantly different from baseline values both in peripheral blood and in PF. Lidocaine significantly decreased severity of CS and inhibited TNF-alpha activity in PF.

Functional walking capacity as an outcome measure of laparoscopic prostatectomy: the effect of lidocaine infusion

Intravenous lidocaine infusion has been shown to affect postoperative pain intensity. This present study was performed to assess the effect of intra- and postoperative lidocaine infusion on postoperative functional walking capacity, as a measure of surgical recovery. Forty patients undergoing laparoscopic prostatectomy were randomized to receive an i.v. infusion of either lidocaine 2 mg kg(-1) h(-1) during surgery and 1 mg kg(-1) min(-1) for the first 24 postoperative hours (lidocaine group) or an equivalent volume of saline 0.9% (control group). All patients received postoperative patient-controlled analgesia with i.v. morphine. Primary outcome was functional walking capacity, as assessed by distance attained during the 2 min walking test (2MWT), recorded daily for the first 3 postoperative days. Morphine consumption and pain intensity were recorded. 2MWT distance decreased by an average of 60% (P<0.01) in both groups on postoperative day 1 (from 150 m before surgery to 53 m), but the decrease was 26 m less in the lidocaine group (P=0.009). During postoperative days 2 and 3, the 2MWT distance increased to an average of 96 m, still 30% less than the preoperative values. There was a significant negative correlation on postoperative days 1 and 2 between the 2MWT distance, pain intensity and fatigue, and morphine consumption. Lidocaine infusion was an independent predictor of the degree of postoperative decrease in 2MWT distance. More patients in the lidocaine group were free from PCA on the second postoperative day (P=0.011). Infusion of lidocaine during surgery and for the first postoperative day attenuated the deterioration in functional walking capacity, and had an opioid sparing effect.

Generalized cortex activation by the auditory midbrain: mediation by acetylcholine and subcortical relays

The inferior colliculus (IC) is a critical component of the ascending projection system carrying auditory information from the brainstem to the forebrain. Recent evidence indicates that, in addition to its role in auditory processing, the IC can exert a generalized, modulatory effect on the forebrain by activating the neocortical electrocorticogram (ECoG). Given the sparse direct projections from the IC to the cortex, it appears that the effect of the IC to produce ECoG activation is indirect, mediated by one or several neuromodulatory systems that have diffuse access to the entire cortical mantle. However, the anatomical relays that permit the IC to influence cortical activity have not been elucidated. In the present experiments, electrical stimulation of the IC suppressed slow, large amplitude oscillations in the ECoG of urethane anesthetized rats, replacing them with higher-frequency cortical activation. This effect was blocked by the muscarinic receptor antagonist scopolamine (0.5-1.0 mg/kg, i.p.), suggestive of a critical role of acetylcholine (ACh) release. Consistent with this hypothesis, localized lidocaine infusions (2%, 1 microl) into the cholinergic basal forebrain complex strongly reduced ECoG activation elicited by IC stimulation. To identify additional relays between the IC and basal forebrain, the effects of lidocaine infusions into the superior colliculus, medial prefrontal cortex, midline thalamus, and dorsal raphe were also studied. Inactivation of the superior colliculus and dorsal raphe reduced IC-induced activation, while prefrontal cortex and thalamic infusions were ineffective. Concurrent basal forebrain and raphe inactivation produced effects similar to that of inactivation of the basal forebrain alone, suggesting that these two areas are arranged in series, rather than acting as independent, parallel pathways. These results suggest that the ability of the IC to induce ECoG activation is mediated, in large parts, by the basal forebrain cholinergic system. Consistent with anatomical evidence, the superior colliculus and dorsal raphe appear to provide important links to functionally connect the IC to the basal forebrain, allowing the IC to indirectly access the entire cortical mantle and enhance processing in neocortical networks.

Synaptic potentiation induced by rTMS: effect of lidocaine infusion

Repetitive transcranial magnetic stimulation (rTMS) delivered at various intensities and frequencies excites cortical motor areas. Trains of stimuli (at 5-Hz frequency, and suprathreshold intensity) progressively increase the size of motor evoked potentials (MEPs) and the duration of the cortical silent period (CSP) in normal subjects. Because antiepileptic drugs, acting mainly on sodium channels, depress MEP facilitation during rTMS, we suggested that rTMS trains facilitate the MEP size by inducing synaptic potentiation primarily involving voltage-gated sodium channels. The aim of this study was to evaluate the effect of lidocaine-a drug that acts selectively on sodium channels-on the rTMS-induced changes in cortical excitability. We tested the changes in motor threshold, MEP size, CSP duration evoked by focal rTMS and the M-wave amplitude in healthy subjects before and after lidocaine infusion. Lidocaine abolished the normal rTMS-induced facilitation of MEPs but left the other rTMS variables and the M-wave unchanged. Our results suggest that the MEP facilitation related to rTMS-induced synaptic potentiation results from an increase in cortical excitatory interneuron excitability that involves voltage-gated sodium channels.

The Effect of Lidocaine Infusion on Morphine Consumption and Pain Control in Burn Patients: 3 N of 1 Studies

The Effect of Lidocaine Infusion on Morphine Consumption and Pain Control in Burn Patients: 3 N of 1 Studies

Selective memory impairments produced by transient lidocaine-induced lesions of the nucleus accumbens in rats.

Reversible lidocaine-induced lesions of the nucleus accumbens (N.Acc.) impaired performance on the spatial win-shift, but not on the cued win-stay, radial arm maze task. Pretraining lesions on the former task did not affect foraging for 4 pellets during either the training or test phases. In contrast, lesions given prior to the test phase significantly disrupted retrieval of 4 pellets on the 8-arm maze. Comparable deficits also were observed in rats trained to forage for 4 pellets on an 8-arm maze without prior win-shift experience. State-dependent drug effects were ruled out by replicating the disruptive effects of lidocaine infusions into the N.Acc. on spatial win-shift performance in rats receiving this treatment prior to both training and test phases. These results suggest that the N.Acc. may interact with the hippocampus to guide foraging behavior requiring memory of previous spatial locations on a maze.

Effects of lidocaine infusion in cats after unilateral labyrinthectomy.

In the auditory/vestibular system, intravenous lidocaine hydrochloride administration has been reported to provide transient relief from severe tinnitus, reduce dizziness and emesis accompanying Meniere's disease, and sometimes improve audiometric thresholds in sensorineural hearing loss. In this study, the labyrinth was destroyed unilaterally in a series of cats. Animals constantly fell and demonstrated prominent contralateral nystagmus and a rotary motion of the head. Within four hours of a 4-mg/kg intravenous lidocaine hydrochloride injection, the cats were able to ambulate freely without falling. The nystagmus was reduced, and there was virtual absence of the rotary head motion. In contrast, the controls had persistent signs of vestibular disturbance. These results demonstrate that lidocaine infusion ameliorates the effects of unilateral labyrinthectomy in cats and thus may be a potential antivertiginous agent.

Effects of Lidocaine Infusion on the Sympathetic Response to Abdominal Surgery

Activation of afferent nerves in the area of surgery is a cause for surgical pain and stress. Intravenous (IV) lidocaine has been shown to inhibit postoperative pain. In the present double-blind study, the effects of a continuous IV infusion of lidocaine (2 mg/min) on the sympathoadrenal stress response to surgery were evaluated in 38 patients scheduled for elective cholecystectomy who were randomly assigned to two groups. In one group, lidocaine infusion was started 30 min before the operation and continued for 24 hr after surgery (n = 18). In the second group (n = 20), saline was infused. The increases in heart rate and blood pressure after tracheal intubation were not significantly different between the groups, but tachycardia and hypertension associated with extubation was prevented in patients given lidocaine. Differences in blood pressure and heart rate between the two groups were otherwise not significant intra- or postoperatively, nor were differences in blood glucose or plasma catecholamine concentrations during the first 24 hr after skin incision. Urinary catecholamine concentrations did not differ significantly in the two groups during the first postoperative day, but during the second postoperative day urinary output of epinephrine and norepinephrine were significantly less in the group of patients receiving lidocaine infusion. It was concluded that the IV infusion of lidocaine during and after major abdominal surgery suppresses extubation-induced hypertension and tachycardia but does not inhibit the general sympathetic response during the first postoperative day. However, lidocaine infusion reduces urinary output of catecholamines during the second postoperative day, suggesting a more rapid decline in the sympathoadrenal response postoperatively in the experimental group.

Effects of lidocaine and epinephrine on myocardial preservation following cardiopulmonary bypass in the dog

The effect of lidocaine infusion on the ultrastructural damage to cardiac muscle by normothermic cardiopulmonary bypass was assessed in nine dogs. Three dogs received no medication other than pentobarbital (30 mg. per kilogram, administered intravenously), and six dogs were treated with lidocaine after anesthesia. Lidocaine was given as a 2 mg. per kilogram loading dose 10 minutes prior to ischemic arrest, followed by a 2 mg. per minute continuous infusion throughout the experimental period. Three of the lidocaine-treated animals received a single injection of epinephrine (0.5 c.c., 1:10,000) immediately after the start of coronary reperfusion. Biopsies of the left ventricular apex were taken after thoracotomy and 5 minutes after the start of coronary reperfusion. In the nontreated dogs, mitochondria were swollen, cristae disrupted, matrix cleared, sarcomeres fragmented, and glycogen was reduced or absent. Ultrastructural damage to dogs receiving lidocaine alone was limited to some swelling of mitochondria, with focal clearing of matrix and disruption of cristae. Generally, sarcomeres were intact and glycogen was present. Ultrastructural changes in dogs receiving lidocaine with epinephrine generally was similar to those in dogs receiving lidocaine alone, with the exception of the mitochondria. In the lidocaine-epinephrine group, the clearing of mitochondrial matrix and disruption of cristae resembled that seen in the nontreated dogs. The results suggest that lidocaine can protect the integrity of the ischemic myocardium and that, even in therapeutic doses, ionotropic drugs can produce ultrastructural changes which might increase the extent of myocardial ultrastructural damage.